BALB/c mice congenic for the C57BL/Ka immunoglobulin (Ig) genes (CB mice) constitute a model animal system in which to study the problem of Ig regulation. We have recently found that production of the IgG2a allotype (G2) in sublethally-irradiated (550 R) CB mice can be chronically suppressed by injecting them with thymocytes from BALB/c donors immune to G2. Further, that G2 suppression is dependent on T cell immunity and can be propagated indefinitely in CB mice by serial transfer of spleen cells. We will test whether BALB/c T cells suppress G2 production in CB mice directly by recognition of G2 determinants on host B cells; or alternatively, whether the G2 suppression of B cells is mediated through a more indirect means and possibly on the basis of an antigen other than G2. Also, we will consider the condition of allotype suppression in CB mice as an immune disorder in B cell differentiation and will test whether a prolonged state of this kind can account for the unexpected cases of leukemia which we observed in G2-suppressed mice.